An arrhythmia is an abnormal heart rhythm. One example of an arrhythmia is bradycardia wherein the heart beats at an abnormally slow rate or wherein significant pauses occur between consecutive beats. Other examples of arrhythmias include tachyarrhythmias wherein the heart beats at an abnormally fast rate. With atrial tachycardia, the atria of the heart beat abnormally fast. With ventricular tachycardia, the ventricles of the heart beat abnormally fast. Though often unpleasant for the patient, an atrial tachycardia is typically not fatal. However, some tachycardia, particularly ventricular tachycardia, can trigger ventricular fibrillation wherein the heart beats chaotically resulting in little or no net flow of blood from the heart to the brain and other organs. Ventricular fibrillation, if not terminated, is fatal. Hence, it is highly desirable to prevent or terminate arrhythmias, particularly ventricular tachycardia.
Assuming an arrhythmia is symptomatically significant, one or more antiarrhythmic cardioactive drugs may be prescribed to prevent or reduce episodes of the arrhythmia. Exemplary cardioactive drugs include Quinidine, Lidocaine, Sotalol, and Ibutilide. These and other cardioactive drugs are classified in the Vaughn-Williams classification system (Table I) according to the method of action. Class I drugs inhibit sodium ion channels in the cellular membrane. Class II drugs act as beta blockers. Class III drugs inhibit potassium channels. Class IV drugs inhibit calcium channels. Details regarding antiarrhythmic drugs are provided in Marcus F. I., Opie L. H. Antiarrhythmic Drugs, in Opie L H (Ed) Drugs for the Heart, Fourth edition, W B Saunders Company, Philadelphia, 1997, pp 207–247, which is incorporated by reference herein.
TABLE IClass IAProcainamide, Quinidine, DisopyramideClass IBLidocaine, Mexiletine, Tocainide, PhenytoinClass ICFlecainide, Propafenone, MoricizineClass IIAcebutalol, Propranolol, EsmololClass IIIBretylium, Amiodarone, Sotalol, IbutilideClass IVVerapamil, Diltiazem, Adenosine
Although antiarrhythmic drugs have been found to be generally effective when prescribed with the appropriate dosage, it is often difficult for the physician to ensure that the appropriate dosage is actually being taken by the patient. Some patients fail to take the prescribed dosage, either intentionally (because they want to avoid perceived side effects of the drug) or unintentionally (because they simply forget to take the drug or run out of the drug). Even if the prescribed dosage of the drug is properly taken, the patient may become immune to effects of drug with time as a result of electrical changes in the heart, development of a new arrhythmia, a myocardial infarction or other factors. On the other hand, a general improvement in the cardiovascular health of the patient as a result of changes to diet or exercise may result in the prescribed dosage becoming unnecessarily strong. In still other cases, the efficacy of a prescribed drug may be affected by conflicts with other drugs. Accordingly, it may be necessary for the patient to frequently visit the physician so that the physician can evaluate the efficacy of the drug and, if necessary, change the dosage or prescribe new or different drugs. Frequent office visits are expensive and inconvenient. Moreover, even with frequent office visits, the physician cannot be completely assured that the correct dosage is applied at all times between office visits. Hence the patient may not be receiving optimal drug therapy at all times.
Another general technique for preventing or reducing episodes of the arrhythmia is to pace or overdrive pace the heart. An implantable cardiac stimulation device, such as a pacemaker, is implanted within the patient to apply electrical pacing pulses to the heart. For bradycardia, the pacemaker may typically be programmed to pace the heart at a rate of 60 to 80 pulses per minute (ppm) to thereby prevent the heart from beating too slowly and to eliminate any long pauses between heartbeats. To prevent tachyarrhythmias from occurring, the pacemaker can be programmed to overdrive pace the heart at a rate faster than the intrinsic heart rate of the patient. Adjustable parameters of the pacemaker are programmed by the physician in an attempt to provide optimal pacing therapy. If antiarrhythmic drugs are also prescribed, programming typically should take into account the efficacy of the drugs. If the drugs are highly effective, generally non-aggressive pacing therapy may be warranted; whereas if the drugs are not very effective, more aggressive pacing therapy should be employed. Hence, changes in the efficacy of antiarrhythmic drugs or changes in the cardiovascular health of the patient may warrant reprogramming of the pacemaker. Frequent office visits are thus also required to ensure pacemakers are optimally programmed based on the possible changes in the efficacy of the antiarrhythmic drugs or other factors. Even with frequent office visits, the physician cannot be completely assured that the optimal programming is provided at all times between office visits. Hence the patient may not be receiving optimal pacing therapy at all times.
For patients at risk of atrial or ventricular fibrillation, an implantable cardioverter defibrillator (ICD) is implanted, which is a device programmed to detect fibrillation and administer an electrical shock to the heart to terminate fibrillation. For atrial tachycardia or fibrillation, antitachycardia pacing or a defibrillation shock may be delivered. For ventricular fibrillation, a defibrillation shock is delivered. If antiarrhythmic drugs are also used, programming of the ICD should preferably take into account the efficacy of the drugs. For example, if antiarrhythmic drugs are not particularly effective, it may be desirable to program the ICD to charge internal capacitors promptly upon detection of slight changes in certain characteristics of the IEGM (internal electrocardiogram) of the patient that indicate a possible imminent ventricular fibrillation, particularly an increase in RT intervals combined with an increase in heart rate. If, instead, the antiarrhythmic drugs are generally effective, slight changes in those IEGM characteristics may not warrant immediate charging of the capacitors. Hence, as with pacemakers, changes in the efficacy of antiarrhythmic drugs or changes in the general cardiovascular health of the patient may warrant reprogramming of the device and frequent office visits may be required to ensure the ICD is optimally programmed at all times.
Thus significant problems can arise as a result of changes in the administration or efficacy of antiarrhythmic drugs. Accordingly, it would be highly desirable to provide techniques with which an implanted cardiac rhythm management device may measure features of cardiac electrical signals typically affected by cardioactive drugs. Note that, herein, the term “event” refers to P-waves, R-waves, etc.; whereas the term “feature” refers to quantifiable aspects of events, such as duration, slope, and time between events or any quantifiable morphology. Furthermore, it is desirable to provide techniques for automatically verifying the administration of particular antiarrhythmic drugs, monitoring the efficacy of the drugs while the patient is out of the clinic and promptly warning the patient or physician (remotely) of any failure to administer the drugs or any significant change in efficacy of the drugs, thus reducing the need for frequent office visits. It would also be desirable to provide a technique for automatically adjusting dosages of antiarrhythmic drugs based on changes in drug efficacy to thereby ensure the optimal dosage at all times. It would also be desirable to provide a technique for automatically adjusting control parameters of a pacemaker or ICD based on changes in drug efficacy to thereby ensure optimal pacing therapy at all times. For patient with ICDs, it would further be desirable to provide a technique for automatically adjusting defibrillation control parameters based on drug efficacy. It is to these ends that the invention is primarily drawn.
Another area in which the automatic monitoring of the efficacy of antiarrhythmic drugs is highly desirable is in connection with patients receiving antiarrhythmic drugs that prolong RT (or QT) intervals, such as Amiodarone or Sotalol. (Conventionally, “QT” refers to the interval between an intrinsic ventricular depolarization event (QRS complex) and the subsequent repolarization (T-wave) as detected within a surface electrocardiogram (ECG). RT refers to substantially the same interval but as detected within the IEGM. The term “RT interval” will be used herein since the invention relates to the processing of IEGM signals rather than ECG signals.) It is crucial patients receiving such antiarrhythmic drugs remain at rest until the RT intervals have returned to a nominal state. Failure to remain at rest can increase heart rate which, in combination with the increased RT intervals, can trigger serious and potentially fatal arrhythmias, such as torsades de pointes or ventricular fibrillation. Typically, patients are required to remain at rest for one to six hours after the drug is administered. For some patients, the RT intervals return to the nominal state more quickly and further rest is not necessary. For other patients, though, the RT intervals do return to the nominal state within six hours and further rest is mandatory. It would be desirable to provide a technique for automatically monitoring the effect of antiarrhythmic drugs on RT intervals to automatically and promptly determine when the patient can resume normal activities. Aspects of the invention are directed to this end as well.